ライフサイエンスコーパス: myelogenous

1 ent of most human cancers, including chronic myelogenous and acute lymphoblastic leukemias initiated

2 s from patients with multiple myeloma, acute myelogenous and lymphoblastic leukemia, and ovarian canc

3 -Abl fusion protein that causes most chronic myelogenous and some acute lymphocytic leukemias (CML an

4 oliferative neoplasms (MPNs) such as chronic myelogenous (CML) and chronic myelomonocytic leukemias (

5 e of immune competence and predisposition to myelogenous diseases in the elderly.

6 d Hep G2), promyelocytic (HL-60) and chronic myelogenous (K-562) leukemias, histiocytic lymphoma (U-9

7 BCR-ABL1, is the defining lesion of chronic myelogenous leukaemia (CML) and a subset of acute lympho

8 l renewal and decreases induction of chronic myelogenous leukaemia (CML) by the BCR-ABL1 oncoprotein.

9 Chronic myelogenous leukaemia (CML) can progress from a slow gro

10 ng the specific survival of the rare chronic myelogenous leukaemia (CML) stem cell population could p

11 ors (TKI) are front-line therapy for chronic myelogenous leukaemia and are among the best-known examp

12 cover' the BCR-ABL1 gene fusion in a chronic myelogenous leukaemia cell line and the TMPRSS2-ERG gene

13 Myelodysplasia resulted and acute myelogenous leukaemia emerged that had acquired several

14 iladelphia chromosome (Ph+)-positive chronic myelogenous leukaemia.

15 level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndr

16 tein levels were robustly expressed in acute myelogenous leukemia (AML) and acute lymphoblastic leuke

17 hosphatase, is overexpressed in 50% of acute myelogenous leukemia (AML) and associated with poor surv

18 potent in vivo anticancer activity in acute myelogenous leukemia (AML) and endemic Burkitt lymphoma

19 by platelet defects, predisposition to acute myelogenous leukemia (AML) and germ-line heterozygous RU

20 ) expression is frequently observed in acute myelogenous leukemia (AML) and has been implicated in le

21 , especially in patients with relapsed acute myelogenous leukemia (AML) and multiple myeloma.

22 PURPOSE Acute myelogenous leukemia (AML) and myelodysplastic syndrome

23 are important for the pathogenesis of acute myelogenous leukemia (AML) and represent a reservoir of

24 Patients with acute myelogenous leukemia (AML) and those undergoing bone mar

25 One patient developed acute myelogenous leukemia (AML) at 6 years of age.

26 a well-defined cohort of patients with acute myelogenous leukemia (AML) at diagnosis and relapse to a

27 ion factor family member, is linked to acute myelogenous leukemia (AML) by chromosomal events at the

28 xpression of IGF1R and IR isoform A in acute myelogenous leukemia (AML) cell lines as well as in >80%

29 ntly, AEG-1 markedly protected HCC and acute myelogenous leukemia (AML) cells from retinoid- and rexi

30 strategies to eradicate primary human acute myelogenous leukemia (AML) cells is a major challenge to

31 eraction between the integrin VLA-4 on acute myelogenous leukemia (AML) cells with stromal fibronecti

32 d panobinostat) were examined in human acute myelogenous leukemia (AML) cells.

33 naling cues in the microenvironment of acute myelogenous leukemia (AML) contribute to disease progres

34 Acute myelogenous leukemia (AML) frequently relapses after com

35 he chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion tra

36 stic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with overexpre

37 (Trib2) is a pseudokinase that induces acute myelogenous leukemia (AML) in mice and is highly express

38 We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexpressio

39 As the pathophysiology of acute myelogenous leukemia (AML) involves a block of myeloid m

40 Acute Myelogenous Leukemia (AML) is an aggressive cancer that

41 Acute myelogenous leukemia (AML) is an aggressive disease asso

42 The microenviroment of acute myelogenous leukemia (AML) is suppressive for immune eff

43 d implement therapeutic approaches for acute myelogenous leukemia (AML) originated primarily from adu

44 toimmune disorders and in NPM1-mutated acute myelogenous leukemia (AML) patients.

45 tate in primary specimens derived from acute myelogenous leukemia (AML) patients.

46 DH1 mutations were identified in 8% of acute myelogenous leukemia (AML) patients.

47 were also screened against M9-ENL1 and acute myelogenous leukemia (AML) primary cell lines and exhibi

48 The survival of most patients with acute myelogenous leukemia (AML) remains poor, and novel thera

49 leukemogenesis in T cells, its role in acute myelogenous leukemia (AML) remains unclear.

50 d next-generation sequencing to assess acute myelogenous leukemia (AML) response to induction chemoth

51 series of 260 newly diagnosed primary acute myelogenous leukemia (AML) samples.

52 ty was observed in four of six primary acute myelogenous leukemia (AML) specimens.

53 ver, the interactions and influence of acute myelogenous leukemia (AML) stem cells with the microenvi

54 regimen that selectively targets human acute myelogenous leukemia (AML) stem cells.

55 Acute myelogenous leukemia (AML) subtypes that result from onc

56 a panel of cell lines representing all acute myelogenous leukemia (AML) subtypes using selective, rev

57 nding protein 2 (SSBP2) is a candidate acute myelogenous leukemia (AML) suppressor gene located at ch

58 9 presented by cell lines, and primary acute myelogenous leukemia (AML) targets that endogenously exp

59 o further accrual after three cases of acute myelogenous leukemia (AML) were reported of a total of 4

60 stic syndrome (MDS) transforms into an acute myelogenous leukemia (AML) with associated increased bon

61 ssion of the MLL-AF9 fusion results in acute myelogenous leukemia (AML) with different behaviors depe

62 topoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone mar

63 Interestingly, patients with acute myelogenous leukemia (AML), acute lymphoblastic leukemia

64 or acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), and chronic myelogenous leuk

65 and clinical outcome of patients with acute myelogenous leukemia (AML), and conventional karyotype-b

66 been implicated in the pathogenesis of acute myelogenous leukemia (AML), but the functional significa

67 Among 5394 cases with acute myelogenous leukemia (AML), the 2-year cumulative incide

68 ssful use of cytotoxic chemotherapy in acute myelogenous leukemia (AML), the biological basis for its

69 In acute myelogenous leukemia (AML), the FLT3 receptor tyrosine k

70 understanding of the genetic basis of acute myelogenous leukemia (AML), we determined the coding exo

71 lt3, an additional important target in acute myelogenous leukemia (AML), with pharmacologically usefu

72 of myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML).

73 nd long-term survival of patients with acute myelogenous leukemia (AML).

74 ll survival (OS) for older adults with acute myelogenous leukemia (AML).

75 ansplantation (alloSCT) in adults with acute myelogenous leukemia (AML).

76 in elderly adults with newly diagnosed acute myelogenous leukemia (AML).

77 nduction chemotherapy for treatment of acute myelogenous leukemia (AML).

78 ients with less-than-favorable risk of acute myelogenous leukemia (AML).

79 ncluding 31 patients with nonremission acute myelogenous leukemia (AML).

80 B, would titrate NK reactivity against acute myelogenous leukemia (AML).

81 overy after intensive chemotherapy for acute myelogenous leukemia (AML).

82 initiating cells (SL-ICs), are rare in acute myelogenous leukemia (AML).

83 in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).

84 The majority of patients (76%) had acute myelogenous leukemia (AML).

85 ineage dysplasia and susceptibility to acute myelogenous leukemia (AML).

86 ssed in subsets of pediatric and adult acute myelogenous leukemia (AML).

87 several human malignancies, including acute myelogenous leukemia (AML).

88 sis in multiple human tumors including acute myelogenous leukemia (AML).

89 rs from 1409 unrelated transplants for acute myelogenous leukemia (AML; n = 1086) and acute lymphobla

90 emotherapy in patients with refractory acute myelogenous leukemia (and other hematologic malignancies

91 nst acute leukemias and blast-crisis chronic myelogenous leukemia (BC-CML).

92 mg twice daily in chronic-phase (CP) chronic myelogenous leukemia (CML) after imatinib treatment fail

93 parts, leukemia stem cells (LSCs) in chronic myelogenous leukemia (CML) and acute myeloid leukemia (A

94 sis in some human cancers, including chronic myelogenous leukemia (CML) and breast cancer.

95 elf-renewal in p210(BCR-ABL)-induced chronic myelogenous leukemia (CML) and exhibits synergistic effe

96 Cancer stem cells lie at the root of chronic myelogenous leukemia (CML) and mediate its continued gro

97 rine fashion, their possible role in chronic myelogenous leukemia (CML) and resistance to imatinib me

98 ment, and prognostic significance in chronic myelogenous leukemia (CML) are largely unknown.

99 We use chronic myelogenous leukemia (CML) as a model of LIC-dependent m

100 repressed in 32D-BCR/ABL, K562, and chronic myelogenous leukemia (CML) blast crisis (BC) primary cel

101 effective therapy for patients with chronic myelogenous leukemia (CML) but is now mostly indicated f

102 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by covalently immobilizing th

103 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine termina

104 Exposure to chronic myelogenous leukemia (CML) caused normal mouse hematopoi

105 Using the K562 chronic myelogenous leukemia (CML) cell line and the doxorubicin

106 ighly active against primary CD34(+) chronic myelogenous leukemia (CML) cells and Ba/F3 cells bearing

107 BCR/ABL kinase-positive chronic myelogenous leukemia (CML) cells display genomic instabi

108 ere assessed in cell-free medium and chronic myelogenous leukemia (CML) cells overexpressing BCR-Abl

109 regulator of imatinib sensitivity in chronic myelogenous leukemia (CML) cells through an unknown mech

110 er65 as RI-mTORC1 signals in primary chronic myelogenous leukemia (CML) cells.

111 A subset of patients with chronic myelogenous leukemia (CML) do not respond to the tyrosin

112 The imatinib paradigm in chronic myelogenous leukemia (CML) established continuous BCR-AB

113 Chronic myelogenous leukemia (CML) in children is relatively rar

114 Chronic myelogenous leukemia (CML) invariably progresses to blas

115 Chronic myelogenous leukemia (CML) is driven by Bcr-Abl, a const

116 Although chronic myelogenous leukemia (CML) is effectively controlled by

117 chromosomal abnormalities (ACAs) in chronic myelogenous leukemia (CML) is generally associated with

118 Effective treatment of chronic myelogenous leukemia (CML) largely depends on the eradic

119 of OBs in regulating normal HSCs and chronic myelogenous leukemia (CML) LSCs.

120 lance of minimal residual disease in chronic myelogenous leukemia (CML) may be relevant for long-term

121 donor lymphocyte infusion (DLI) for chronic myelogenous leukemia (CML) may result from immunologic a

122 ukemias in recipient mice resembling chronic myelogenous leukemia (CML) myeloid blast crisis.

123 effective in inducing remissions in chronic myelogenous leukemia (CML) patients but do not eliminate

124 We previously demonstrated that chronic myelogenous leukemia (CML) patients treated with DLI dev

125 Chronic myelogenous leukemia (CML) patients treated with imatini

126 g primitive leukemic precursors from chronic myelogenous leukemia (CML) patients.

127 changed the therapeutic strategy for chronic myelogenous leukemia (CML) patients.

128 uces the burden of leukemia cells in chronic myelogenous leukemia (CML) patients.

129 se gene signatures in cell lines and chronic myelogenous leukemia (CML) patients.

130 bility to chromosomal aberrations in chronic myelogenous leukemia (CML) progenitors after exposure to

131 Chronic myelogenous leukemia (CML) results from a chromosomal tr

132 Chronic myelogenous leukemia (CML) results from transformation o

133 ely active mutant of Abl that causes chronic myelogenous leukemia (CML) stimulated the expression and

134 Progression of chronic myelogenous leukemia (CML) to accelerated (AP) and blast

135 ia stem cells (LSC) in chronic phase chronic myelogenous leukemia (CML) using a transgenic mouse mode

136 selenium has been shown to alleviate chronic myelogenous leukemia (CML) via the elimination of leukem

137 e in CLL, GRN was not upregulated in chronic myelogenous leukemia (CML) where miR-107 paralogs are no

138 ction (QPCR) levels in patients with chronic myelogenous leukemia (CML) who are in complete cytogenet

139 Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase

140 During blast crisis of chronic myelogenous leukemia (CML), abnormal granulocyte macroph

141 imatinib is remarkably effective in chronic myelogenous leukemia (CML), although drug resistance is

142 complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an imm

143 a major role in the pathogenesis of chronic myelogenous leukemia (CML), and is the target of the bre

144 highly effective in the treatment of chronic myelogenous leukemia (CML), but primary and acquired res

145 hibitors are effective therapies for chronic myelogenous leukemia (CML), but these inhibitors target

146 se inhibitors (TKIs), a treatment of chronic myelogenous leukemia (CML), has largely replaced curativ

147 eted therapies, such as imatinib for chronic myelogenous leukemia (CML), represent the first agents t

148 b at inhibiting Bcr-Abl and treating chronic myelogenous leukemia (CML), resistance to the therapy oc

149 ncogene homolog 1 (BCR-ABL1)-induced chronic myelogenous leukemia (CML)-like myeloproliferative neopl

150 ntestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

151 e chronic and blast crisis phases of chronic myelogenous leukemia (CML).

152 iescent leukemia stem cells (LSC) in chronic myelogenous leukemia (CML).

153 in patients with advanced stages of chronic myelogenous leukemia (CML).

154 the treatment of imatinib-resistant chronic myelogenous leukemia (CML).

155 kinase inhibitor (TKI) therapies in chronic myelogenous leukemia (CML).

156 tial mediator of the pathogenesis of chronic myelogenous leukemia (CML).

157 a causative tyrosine kinase (TK) of chronic myelogenous leukemia (CML).

158 successful front-line treatment for chronic myelogenous leukemia (CML).

159 tiated by the BCR-ABL1 kinase causes chronic myelogenous leukemia (CML).

160 R-ABL inhibitor imatinib in treating chronic myelogenous leukemia (CML).

161 esis of many human cancers including chronic myelogenous leukemia (CML).

162 /progenitor cells from patients with chronic myelogenous leukemia (CML).

163 nase inhibitor that is used to treat chronic myelogenous leukemia (CML).

164 ine kinase inhibitors and relapse of chronic myelogenous leukemia (CML).

165 gene networks that are important for chronic myelogenous leukemia (CML).

166 ntestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

167 ine kinase (BCR-ABL) oncogene causes chronic myelogenous leukemia (CML).

168 stability, leading to development of chronic myelogenous leukemia (CML).

169 ors (TKI) have improved treatment of chronic myelogenous leukemia (CML); however, most patients are n

170 and revolutionized the treatment of chronic myelogenous leukemia (CML); in 2006 and 2007, approval o

171 e long-term response in blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosom

172 ss of miR-328 occurs in blast crisis chronic myelogenous leukemia (CML-BC) in a BCR/ABL dose- and kin

173 Leukemic stem cells in chronic phase chronic myelogenous leukemia (CP-CML) are responsible for diseas

174 half of patients with chronic-phase chronic myelogenous leukemia (CP-CML) in complete molecular resp

175 leukemia (GVL) against chronic-phase chronic myelogenous leukemia (CP-CML) is potent, but it is less

176 SCT) is potent against chronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-

177 used the experimental data from immortalised myelogenous leukemia (K562) and healthy lymphoblastoid (

178 amster Ovary (CHO) cells, Human Immortalized Myelogenous Leukemia (K562) cells and hematopoietic stem

179 cs of DNA damage by 1 and 3 in human chronic myelogenous leukemia (K562) cells.

180 l lines isolated from a patient with chronic myelogenous leukemia (KBM7 and HAP1), as well as haploid

181 mples from 15 myelodysplastic syndrome/acute myelogenous leukemia (MDS/AML) patients undergoing decit

182 cute myelogenous leukemia (AML), and chronic myelogenous leukemia (RR = 26.9, 66.5, and 93.1, respect

183 tive neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes h

184 Therapy-related acute myelogenous leukemia (t-AML) is an important late advers

185 -related myelodysplastic syndromes and acute myelogenous leukemia (t-MDS/AML) comprise an increasingl

186 Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complicatio

187 t myeloid leukemia blasts (including chronic myelogenous leukemia [CML]-blast crisis cells) rely on c

188 both acute lymphoblastic leukemia and acute myelogenous leukemia achieve remission with upfront chem

189 We report a patient with relapsed acute myelogenous leukemia after allogeneic stem cell transpla

190 re previously avoided in patients with acute myelogenous leukemia aged more than 55 years because of

191 Here, we identify two patients with acute myelogenous leukemia and B-cell acute lymphoblastic leuk

192 s the history of transplantation for chronic myelogenous leukemia and defines the new natural history

193 The trail blazed by imatinib for chronic myelogenous leukemia and GIST has become a desired route

194 increasing the time to progression to acute myelogenous leukemia and improving overall response rate

195 of inactivating mutations of DNMT3A in acute myelogenous leukemia and myelodysplastic syndrome, our r

196 erapeutic response for patients with chronic myelogenous leukemia and Philadelphia chromosome-positiv

197 ioned drug candidates against breast cancer, myelogenous leukemia and prostate cancer by looking for

198 94 and 88 candidate drugs for breast cancer, myelogenous leukemia and prostate cancer, 32%, 13% and 1

199 ndous impact on clinical outcomes in chronic myelogenous leukemia and revolutionized the field of tar

200 xpressed in breast cancer), BCR-ABL (chronic myelogenous leukemia and some cases of acute lymphoblast

201 ole caregiver for her husband, who has acute myelogenous leukemia and was undergoing allogeneic hemat

202 therapies and immune checkpoint therapies in myelogenous leukemia are desired.

203 genic KIT in systemic mastocytosis and acute myelogenous leukemia are poorly understood.

204 oblastic leukemia (ALL) and lymphoid chronic myelogenous leukemia blast crisis.

205 This procedure remains an option in chronic myelogenous leukemia but its use will become more sparin

206 mic blasts isolated from patients with acute myelogenous leukemia but was relatively sparing of norma

207 the clinical outcome for patients with acute myelogenous leukemia by reducing the incidence of leukem

208 nd broad H3K4me3 domains in the K562 chronic myelogenous leukemia cell line as well as the MCF-7 brea

209 dentify essential genes in the human chronic myelogenous leukemia cell line K562.

210 ere cellular membrane fragments of a chronic myelogenous leukemia cell line, KU-812, were immobilized

211 ilar to native GCSF using the mouse M-NFS-60 myelogenous leukemia cell line.

212 s Crk was robustly phosphorylated in chronic myelogenous leukemia cell lines and in A431 and MDA-MB-4

213 they potently induced cell death in chronic myelogenous leukemia cell lines.

214 eration of the effects of As(2)O(3) on acute myelogenous leukemia cells and raise the potential of mo

215 TF-1 erythroleukemia and primary human acute myelogenous leukemia cells in vitro.

216 Treatment of K562 chronic myelogenous leukemia cells with phorbol-12-myristate-13-

217 e that Id genes are expressed in human acute myelogenous leukemia cells, and that knock down of Id1 e

218 n of hematopoietic stem/progenitor and acute myelogenous leukemia cells.

219 ential for development and survival of acute myelogenous leukemia cells.

220 s with acute lymphoblastic leukemia or acute myelogenous leukemia compared with normal bone marrow.

221 A 33-year-old woman with chronic myelogenous leukemia developed widespread alopecia invol

222 cell transplantation was the goal in chronic myelogenous leukemia for over 20 years and remains an op

223 PURPOSE Patients with chronic myelogenous leukemia in accelerated phase (CML-AP) that

224 nd in CD34+ cells from patients with chronic myelogenous leukemia in blast crisis.

225 lated tyrosine kinase BCR-ABL causes chronic myelogenous leukemia in humans and forms a large multipr

226 amily kinase inhibitor used to treat chronic myelogenous leukemia in humans.

227 eased risk of development of secondary acute myelogenous leukemia involving the mixed-lineage leukemi

228 Successful treatment of chronic myelogenous leukemia is based on inhibitors binding to t

229 Acute myelogenous leukemia is propagated by a subpopulation of

230 Chronic myelogenous leukemia is typified by constitutive activat

231 of human tumor cell lines and clinical acute myelogenous leukemia isolates, which express abundant PK

232 in lymphohematopoietic cell lines and acute myelogenous leukemia isolates.

233 ukemia virus or those expressing the chronic myelogenous leukemia oncoprotein BCR-ABL in the hematopo

234 ary blasts isolated from patients with acute myelogenous leukemia or acute lymphocytic leukemia.

235 ears (range, 18-69 years), and 95% had acute myelogenous leukemia or high-risk myelodysplastic syndro

236 as well as in the majority of primary acute myelogenous leukemia patient samples.

237 ne kinase FLT3 are frequently found in acute myelogenous leukemia patients and confer poor clinical p

238 acinus are overexpressed in some human acute myelogenous leukemia patients and correlate with elevate

239 ue, we analyzed outcomes of 2223 adult acute myelogenous leukemia patients who underwent allogeneic H

240 gene give rise to drug resistance in chronic myelogenous leukemia patients.

241 and primary leukemic progenitors from acute myelogenous leukemia patients.

242 cluding therapy-refractory B-ALL and chronic myelogenous leukemia samples, and inhibits growth of hum

243 corepressors originally identified in acute myelogenous leukemia that have recently been linked to e

244 orrelates with sensitivity of clinical acute myelogenous leukemia to chemotherapy, whereas low BAK le

245 -Abl tyrosine kinase associated with chronic myelogenous leukemia to small molecule inhibitors that t

246 Finally, in patients with acute myelogenous leukemia treated with hematopoietic stem cel

247 e been reported in patients who have chronic myelogenous leukemia treated with the tyrosine kinase in

248 In human acute myelogenous leukemia we showed that all preleukemic muta

249 1 case in which neoplastic cells of chronic myelogenous leukemia were intermingled with the cells of

250 ed by the Philadelphia chromosome in chronic myelogenous leukemia were unraveled, and these have led

251 ders, 7 nonresponders) with relapsed chronic myelogenous leukemia who received CD4(+) DLI in the pre-

252 one marrow or peripheral blood HCT for acute myelogenous leukemia, acute lymphoblastic leukemia, chro

253 tive anaplastic large cell lymphoma, chronic myelogenous leukemia, and acute leukemias.

254 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome betwe

255 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome enrol

256 ified as chromosomal translocations in acute myelogenous leukemia, are transcriptional corepressors t

257 IDH1), frequently found in gliomas and acute myelogenous leukemia, creates a neoenzyme that produces

258 atment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression and i

259 n patients developed myelodysplasia or acute myelogenous leukemia, four of those being the rare but u

260 R-ABL inhibitor for the treatment of chronic myelogenous leukemia, has created a great impetus for th

261 well-known therapeutic agent against chronic myelogenous leukemia, is an effective inhibitor of Abl t

262 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, or myelodysplastic syndrome; 98% r

263 he BCR-Abl translocation involved in chronic myelogenous leukemia, reportedly produces alopecia accor

264 ma, colorectal and prostate cancers, chronic myelogenous leukemia, small cell lung cancer, and medull

265 In chronic myelogenous leukemia, the constitutive activation of the

266 (-/-) mouse model of engrafted human chronic myelogenous leukemia, we now demonstrate the complete el

267 Using a murine model of chronic myelogenous leukemia, we show that malignant and nonmali

268 ntiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs), thereb

269 m a very early age a more aggressive chronic myelogenous leukemia-like disease than mice deficient in

270 rosine kinase inhibitor approved for chronic myelogenous leukemia.

271 lance and result in the development of acute myelogenous leukemia.

272 ces similar survival for patients with acute myelogenous leukemia.

273 milar survival times for patients with acute myelogenous leukemia.

274 in patients with imatinib-resistant chronic myelogenous leukemia.

275 transform to myelodysplastic syndrome/acute myelogenous leukemia.

276 re implicated in leukemias, especially acute myelogenous leukemia.

277 n a syndrome highly similar to human chronic myelogenous leukemia.

278 inib for the first-line treatment of chronic myelogenous leukemia.

279 eukemic progenitors from patients with acute myelogenous leukemia.

280 some hematopoietic cancers, such as chronic myelogenous leukemia.

281 ainst a mouse model of chronic-phase chronic myelogenous leukemia.

282 a substrate of the BCR-ABL kinase in chronic myelogenous leukemia.

283 nificant activity in patients with MDS/acute myelogenous leukemia.

284 the current role of the procedure in chronic myelogenous leukemia.

285 arnib exhibits modest activity against acute myelogenous leukemia.

286 titutively active kinase that causes chronic myelogenous leukemia.

287 incidence of myelodysplastic syndrome/acute myelogenous leukemia.

288 in the development of both acute and chronic myelogenous leukemia.

289 n 6 years after HCT for treatment of chronic myelogenous leukemia.

290 hematopoietic cell transplantation for acute myelogenous leukemia.

291 n chromosome translocations that cause acute myelogenous leukemia.

292 nic fusion protein characteristic of chronic myelogenous leukemia.

293 xtended life to the degree seen with chronic myelogenous leukemia.

294 as the cause of some familial cases of acute myelogenous leukemia/myelodysplastic syndrome and in Mon

295 Acute myelogenous leukemias (AMLs) and endothelial cells depen

296 on kinase is the driving mutation of chronic myelogenous leukemias and is also expressed in a subset

297 condary glioblastomas, and a subset of acute myelogenous leukemias but have not been detected in othe

298 optosis of CSC derived from chronic or acute myelogenous leukemias when administered at supraphysiolo

299 lymphoblastoid B cell (GM12878) and chronic myelogenous leukemic (K562) ENCODE Tier 1 cell lines.

300 Despite positive staining, acute myelogenous leukemic cells were not killed by IMMU-114.